watch your cerratines, those are kidneys, Again the best person to give you advice on the forum concerning all things transplant is Mike Simon,
Your levels are just barely out of range, try and relax,
If you could reduce your Prograf dose your kidney function might improve some.
I don't know anything about you but at 4 years out your anti-rejection regimen seems rather aggressive. As I understand you you're taking 4 mg Prograf a day and 1000 mg Cellcept. I am 8 years out and I'm taking 2 mg Prograf in the am and 1 mg in the pm. I was taking 2 mg Prograf a day at 5 years out and then they tried to wean me off Prograf completely (2 mg one day then nothing the next and 2 mg the next and nothing the next and so on) and I think I had a minor component of rejection and increased my dose to 3 mg per day, I think I'd ask about the possibility of reducing the Prograf and see how that goes. I believe that any dose change in the anti-rejection regimen should be accompanied by fequent labs until you see that everything is stable. I insist on weekly labs since I got into trouble with my last dose adjustment.
Your liver enzymes are out of range but not significantly so. Perhaps if you had a biopsy and it looked good you would relax a bit. Without knowing your liver architecture I can't suggest treatment for HCV. I hope that Telepravir becomes accessible soon and transplant recipients will be able to get it. If your liver histology is good perhaps waiting is a good approach. Your enzymes alone are not remarkable and on that basis I would guess that your liver is in pretty good shape. A biopsy is the only way to know for sure and I assume you've had enough of those that they don't scare you much. They don't me - except for that results, that is.
Thank you so very much for responding. I will talk to my Dr regarding lowering my prograf ASAP. The Dr I have now is new, I just basically fired my old Dr. He had me stop taking cellcept and with in 30 days I went into rejection after being stable for so long. My new Dr. told me that was a bad decision and I will probably be on cellcept for the rest of my life. I understand that there is a cocktail on the way similar to HIV meds that have so far shown good results in trials. I am also a participant at (NIH) Nat'l Institute of Health. The cocktail will consist of pegalated iterferon/ribaviron and some protese inhibitors. This is for non responders. I am a geno type 1b. Interferon has never worked for me since 1992 and I have been on them all. Thankyou...GOD BLESS!!!
I agree with Mike, you seem to be on too much of anti-rejection meds. One way to know is to test prograf levels in your blood which you probably do. But you mentioned that your doctor is new, is he experienced enough? Can you get a second opinion from an reputable hepatologist?
Cellcept is a strong drug and as far as I know it has more side effects than prograf. I am taking now (6 years after TP) 1.5 mg of prograf and 1 mg of rapamune per day. The latter is considered also to have some antiviral effect. However, different people metabolize drugs differently, so it has to be decided based on lab tests.
You take now 4 mg of program and 1000 mg of cellcept, which seems to be a large dose. You need to make sure that you are not oversuppressed, so have a second opinion from an experienced hepatologist. If the change of dose is recommended, it has to be slow and closely monitored as Mike suggested. Best of luck to you. Jeff.
Thanks for responding Jeff. After my transplant 4 years ago at University of Maryland Med. Cntr. While I was still under the care of my surgeons we went through trial and error to determine my meds. I was on 250mg of cellcept and 2 mg of prograf....it had to be increased. Then we went to 500mg of cellcept and 2mg of prograf...it got better. Then we went to 500mg of cellcept and 4mg of prograf and this is where I have been since then. My surgeons told me that I have a very strong immune system and all systems are different. They even told me that most people take less. After the surgeons feel that you are stable they let you go. Now you must find someone to monitor your care and blood work. I get blood work done every 2 months now. I have been through several Dr's believe it or not a lot of these guy do not know what they are doing. My new Dr. told me that the longer you are out there your body changes and therefore your med must change as well. Lets face it these meds will eventually destroy you kidneys. I saw a nephrologist(kidney Dr.) and she told me that I had already lost 48 percent of my kidney functions due to the meds. This lost cannot be recovered. It seems that when lowering the meds the creatinine lvls(kidney functions) drop some what but the ALT/AST increases so there has to be a balance. Seems like I cant win for losing. If this continues I will have to get dialisys treatment or go on a kidney transplant list. You know the higher your AST/ALT gets the more scaring occures and in most cases hep C can be very aggressive after transplant. So I salute those that has over come hep C. Even if interferon works for me and it has not yet I still have to take the meds. which is slowly destroying my kidneys. Unfortunately we all are in the same boat some will take much much longer because there meds are not as high as mine. That is why I watch these clinical trials so closely at (NIH). I have been dealing with Gastroenterologist, I think I'm going to switch to a Hepotologist they may be better at dealing with these med changes....GOD BLESS!!......Dan
My understanding is that Cellcept is easier on the kidneys than Prograf. I am not certain but I think Sirilimus(Rapamune) is as well.
I am curious whether your nephrologist had you do a 24 hour urine test or if she only looked at your creatinine level and eGFR (estimated glomerular filtration rate). I ask this because my surgeon told me that blood creatinine level is not as reliable a marker in the transplant community and it is in the general population and particularly in recipients over 50. My creatinine was around 1.4 and when he saw the results of my 24 urine test he said I was fine. I never researched that issue so I don't know how accurate that premise is.
I agree that a hepatologist would probably be a better choice but I would want one familiar with liver transplantation. When you're fooling with anti-rejection drugs you want a doctor very knowledgeable about that stuff. I find it strange that you aren't followed by someone at your transplant center. Perhaps I misunderstood you and you are. I am still treated by my transplant surgeon so that's really all I have known.
You said that you didn't respond to interferon. Have you treated since your transplant? I ask because I have seen articles which state that the response can change after transplantation and some patients who were not responsive to Peg/Riba pre-transplant do respond post-transplant. I could probably find something about that if you are interested.
The possibility of change in response to interferon after transplant is real. I treated twice before TP and in both cases after 3 months of tx my liver enzymes would shoot up and I had to quit. After TP, I started responding. As I said, I was und at about 24 wks. Jeff.
Thankyou guys....there is truely a GOD! Regarding Peg/Rib I have not tried it yet because I was begining to feel that I was one of those that would never respond and I was not going to be some Dr's ginny pig again as I stated earlier I have tried all interferons since 1992 and by the grace of GOD I weathered the storm. You know interferon is no joke it can @%!*$ you up. I have gotten fired off my job while on interferon so I have a big history with it so NOW I make absolutely sure before I take a chance with it these days so this is truely good news for me. As far as Cellcept Mike you are right it is easy on the kidneys. It's the prograf that's the culprit here. I have a friend that only takes the liquid form because 1mg was too much for him....lucky devil. Is Rapamune similar to prograf? You know now that I have talked with you I feel that maybe my meds can be altered altogether and yes I went through the entire process for kidney testing, bood work, 24 hr. urinalisys the works. Now you know you can survive on one kidney and basically thats what I have the equivalent of, but with my exercise and diet program...(not Dr. prescribed) I'm a health freak I really dont feel the effects of my reduced kidney functions. I read blood work like a specialist and I have all my labs sent to me. My creatinine levels used to be 1.4 four years ago and thats high. I know that 1.5 is the max but a nephrologist will explain to you that damage has already occured so do the math if I was 1.4 four years ago and I'm now almost 1.9 you have to admit this is not good so changing these meds is critical for me. There are trials going on right now to get us off of these meds, the imune system must accept our new livers or we will always be very very acceptable to every bad germ, bacteria and desease thats out there. Again guys thank you very much. I have learned a lot and will execute immediately....GOD BLESS!!.......Dan
Rapamune is Sirilimus and I believe it is easier on renal function. Google and see what you find. I was on the drug for a while and I wanted to stop but I cannot recall why. I think I was probably treating my HCV and since I felt so bad I likely blamed every drug I was taking and tried anything to feel better. I might ask about it now because my kidney function isn't ideal, by any means. I will research it and we can share what we find.
Mike, Jeff and (anyone out there on anti rejection meds)
Creatinine (Renal/Kidney) level of more than 1.2 and depends on which lab/center you go to 1.5 are concidered max levels for renal/kidney fuctions of course seeing a nephrologist will give you the true and most acurate dianostics of your renal functions. Before I was transplanted my levels were normal. They were under .99 about 6 years ago. After my transplant 4 years ago I started these meds my levels slowly increased they were 1.4. They are now today 1.89. I was informed that this is ENEVITABLE WITH ALL LIVER TRANSPLANTS on immune suppressant especially prograf. My nephrologist (renal/kidney specialist) confirmed that my kidneys are failing due to the meds.
IS ANYONE ELSE OUT THERE HAVING THE SAME PROBLEMS!!!!!!!!!!!!
Have you checked or noticed. Those who have been on meds for a while, What are your current levels? I found this information on the internet about kidney failures.
Renal failure or kidney failure is a situation in which the kidneys fail to function adequately. It is divided in acute and chronic forms; either form may be due to a large number of other medical problems.
Biochemically, it is typically detected by an elevated serum creatinine. In the science of physiology, renal failure is described as a decrease in the glomerular filtration rate. When the kidneys malfunction, problems frequently encountered are abnormal fluid levels in the body, deranged acid levels, abnormal levels of potassium, calcium, phosphate, hematuria (blood in the urine) and (in the longer term) anemia. Long-term kidney problems have significant repercussions on other diseases, such as cardiovascular disease.
1 Acute renal failure
2 Chronic kidney disease
3 Acute on chronic renal failure
Renal failure can broadly be divided into two categories: acute or chronic renal failure. The type of renal failure is determined by the trend in the serum creatinine. Other factors which may help differentiate acute and chronic kidney disease include the presence of anemia and the kidney size on ultrasound. Chronic kidney disease generally leads to anemia and small kidney size.
Acute renal failure:
Acute renal failure (ARF) is, as the name implies, a rapidly progressive loss of renal function, generally characterized by oliguria (decreased urine production, quantified as less than 400 mL per day in adults, less than 0.5 mL/kg/h in children or less than 1 mL/kg/h in infants); body water and body fluids disturbances; and electrolyte derangement. An underlying cause must be identified to arrest the progress, and dialysis may be necessary to bridge the time gap required for treating these fundamental causes. ARF can result from a large number of causes.
Chronic kidney disease:
Stage 5 Chronic Kidney Disease (CKD) can either develop slowly and show few initial symptoms, be the long term result of irreversible acute disease or be part of a disease progression.
Acute on chronic renal failure
Acute renal failure can be present on top of chronic renal failure. This is called acute-on-chronic renal failure (AoCRF). The acute part of AoCRF may be reversible and the aim of treatment, as with ARF, is to return the patient to their baseline renal function, which is typically measured by serum creatinine. AoCRF, like ARF, can be difficult to distinguish from chronic renal failure, if the patient has not been monitored by a physician and no baseline (i.e., past) blood work is available for comparison.
Causes of Acute Kidney Disease:
Acute kidney failure usually occurs as the result of a sudden interruption in the blood supply to the kidney, or as a result of a toxic overload of the kidneys. Some causes of acute failure include accidents, injuries or complications from surgery where the kidneys are deprived of normal blood flow for an extended period of time. Heart-bypass surgery is an example of a situation in which the kidneys receive reduced blood flow.
Drug overdoses, whether accidental or from chemical overloads of drugs such as antibiotics or chemotherapy, may also cause the onset of acute kidney failure. Unlike in chronic kidney disease, however, the kidneys can often recover from acute failure, allowing the patient to resume a normal life. People suffering from acute failure require supportive treatment until their kidneys recover function, and they often remain at an increased risk of developing future kidney failure.
Causes of Chronic Kidney Disease:
There are many causes of CKD. The most common cause is diabetes mellitus. The second most common cause is long-standing, uncontrolled, hypertension. Polycystic kidney diease is also a well known cause of chronic kidney disease. The majority of people afflicted with polycystic kidney disease have a family history of the disease. Many other genetic illnesses also affect kidney function. Overuse of some common drugs, such as aspirin, ibuprofen and acetaminophen can also cause chronic kidney damage.
Methods of Measurement for CKD
Stages of Kidney Failure
Chronic kidney failure is measured in five stages, which are calculated using a patient’s GFR, or glomerular filtration rate. Stage 1 CKD is mildly diminished renal function, with few overt symptoms. Stages 2 and 3 need increasing levels of supportive care from their medical providers to slow and treat their renal dysfunction. Patients in stages 4 and 5 usually require preparation of the patient towards active treatment in order to survive.Stage 5 CKD is considered a severe illness and requires some form of renal replacement therapy (dialysis) or kidney transplant whenever feasible.
Glomerular Filtration Rate
A normal GFR varies according to many factors, including sex, age, body size and ethnicity. Renal professionals consider the glomerular filtration rate (GFR) to be the best overall index of kidney function. The National Kidney Foundation offers an easy to use on-line GFR calculator at the following webpage[] for anyone who is interested in knowing their glomerular filtration rate.(A serum creatinine level, a simple blood test, is needed to use the calculator).
Use of the term uremia
Before the advancement of modern medicine, renal failure was often referred to as uremic poisoning. Uremia was the term used to describe the contamination of the blood with urine. Starting around 1847, this term was used to describe reduced urine output, that was thought to be caused by the urine mixing with the blood instead of being voided through the urethra. The term uremia is now used to loosely describe the illness accompanying kidney failure.
Sorry guys I know we have already discussed this and I am talking to my doctor about
lowering my prograf but this question is mainly concerning a long term solution/resolution
Mycophenolate mofetil monotherapy in patients who underwent liver transplantation for hepatitis C cirrhosis.
Manrique A, Jiménez C, Ortega P, Abradelo M, Gimeno A, Calvo J, Cambra F, -Sterup RL, Morales JM, Moreno E.
Alejandro Manrique Municio, Hospital Doce de Octubre, Servicio de Cirugía General, Madrid, Spain.
INTRODUCTION: Mycophenolate mofetil (MMF) monotherapy has recently been proposed for liver transplant recipients with adverse events (nephrotoxicity, hypertension) related to calcineurin inhibitors. We analyzed the influence of MMF on the clinical course of recurrent hepatitis C. METHODS: Among 1038 patients who underwent liver transplantation (OLT) from April 1986 to October 2006, we analyzed 48 adult recipients (4.6%) whose diagnosis was hepatitis C virus (HCV) cirrhosis and who were converted from calcineurin inhibitors to MMF monotherapy. RESULTS: The 36 men and 12 women, had a mean age at OLT of 52.9 +/- 7.2 years; the time elapsed from OLT to the onset of MMF monotherapy was 72.5 +/- 47.6 months (range = 11-210). The mean follow-up after monotherapy was 19 +/- 16.1 months (range = 2-67). Indications for conversion were: chronic renal dysfunction with HCV in 45 patients; HCV recurrence in two; and hypertension plus HCV recurrence in one subject. When the indication was renal dysfunction (excluding three patients who underwent hemodialysis), the mean creatinine values decreased significantly from baseline to 6 months of monotherapy from 1.63 +/- 0.61 mg/dL to 1.51 +/- 0.78 mg/dL (P < .03). The creatinine clearance only improved significantly from the baseline value of 56.6 +/- 16.8 mL/min to the value at 3 months of monotherapy-63.6 +/- 18.4 mL/min (P < .001). At the last outpatient visit, creatinine and creatinine clearances had not changed significantly. The mean diastolic blood pressure did improve significantly at the end of the study. The mean glucose levels decreased but not significantly at the last outpatient visit. Liver function tests did not change significantly after conversion to MMF monotherapy. The acute rejection rate was 8.3%, and adverse events related to MMF monotherapy were present in 9 patients (18.7%). CONCLUSIONS: Conversion from calcineurin inhibitors to MMF monotherapy in patients who underwent OLT for HCV transiently improved renal function and hypertension. The acute rejection rate was low, and adverse events were usually well tolerated.